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Mottram et al. (1) recently reported in the Journalnew and unexpected findings: that a hypertensive response to exercise (systolic blood pressure >210 mm Hgin males and >190 mm Hg in females) in normotensive and hypertensive subjects is associated with subtle defects in systolic left ventricular (LV) function. A number of possible mechanisms were proposed.

Another explanation, not canvassed, relates to the effects of wave reflection on the pattern of systolic LV ejection, and on amplification of the aortic pressure wave to the site of pressure recording in the brachial artery.

Amplification of the pressure wave to the brachial or radial artery can be substantial during exercise, with one study showing peak difference of 80 mm Hg between aortic and radial peak pressure during maximal exercise (2). The degree of amplification depends on ejection period, being greatest when this is short, and least when it is long (3–5). Amplification of the pulse wave is attributable to wave reflection within the upper limb (3–6).

Most wave reflection returning to the heart comes from the lower part of the body (trunk and lower limbs) (6). This appears to be maintained during exercise in patients with systolic LV dysfunction (7). However, effects of wave reflection on the heart depend on the ability of the heart to eject against pressure. With impaired LV contractility, reflection has a greater effect on flow than pressure (8), and this restricts late ejection, causing shortened ejection, with accompanying decrease in stoke volume. The shortened ejection in severe heart failure is responsible for absence of systolic augmentation and appearance of the classic “dicrotic” pulse waveform (6,9).

It is quite possible that this mechanism is responsible for the findings of Mottram et al. (1), namely that increased wave reflection during the challenge of exertion causes greater reduction than usual in ejection duration, and that this leads to greater amplification of the pulse in the upper limb, and a greater recorded systolic pressure in the upper limb.

Finally, such a hypothesis could be tested by measuring ejection duration during exercise, and/or by estimating the aortic systolic pressure from the upper limb waveform. Have the investigators considered measuring ejection duration or central systolic pressure?

Footnotes

↵1 Please note: Dr. O'Rourke is the Director of Atcor Medical, manufacturer of instruments for analysing the arterial pulse.

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